Perforated gastric lymphoma

75 year old gentleman recently diagnosed with B-cell lymphoma, staged with CT scan which showed only extensive para-aortic lymphadenopathy and no visceral disease received his first dose of chemotherapy late last week. Six hours later he presented with a perforation involving the greater curvature of the fundus. No mass was palpable, so I mobilized the greater curvature and resected and closed the area of perforation with a TA-90 stapler. Exploration also revealed a friable lesion of the proximal jejunum that appeared on the verge of perforation, so I resected this and placed a gastrostomy and jejunostomy.

Post op course has been stormy. He has run a persistent hyperchloremic metabolic acidosis with compensatory respiratory alkalosis despite good oxygenation and a high urine output (urine osmolality 476, serum osmolality 324, urine Na < 10, serum Na 150). Pathology came back today and reveals lymphoma in the gastric specimen, small bowel specimen and even in some adjacent omentum, which was resected because its viability looked questionable.

Questions:

1. What is the risk of another perforation with probable residual lymphoma at the resection margin? Would anyone go back and resect more stomach at this point?

2. Why the persistent metabolic acidosis? He does not appear to be septic, (abdomen soft, not tachy, good urine output), but of course that is always a possibility given the recent chemo He did receive Neupogen). He had severe hypercalcemia on presentation (14.5), treated with IV Aredia and saline, but his calcium has subsequently been normal.

3. Does anyone think that the chemo caused the perforation in only 6 hours, or was this lesion headed towards spontaneous perforation before the chemo was given, perhaps explaining the tumor cells in the omentum?

I don’t have much experience with GI lymphoma, but in meditereanian lymphoma, which commonly invloves the GI tract, perforation is very unusual. I don’t think a new operation is warranted, but I am anxious to read what others have to say on this.

As to the metabolic acidosis, you say that the metabolic acidosis is hyperchloremic (or normal anion gap). Such metabolic acidosis is caused by bicarbonate loss somewhere. There are only two possible sites: the GI tract, or the kidneys.

I don’t think that the GI tract is a problem. For that you need either a duodenal or pancreatic fistula, (very rarely high jejunal fistula) or severe diarrhea, which your patients has not. (I presume the gastrostomy is not putting out too much, and that what it is putting out is acidic).

So we are left with renal tubular acidosis.

Many drugs can cause renal tubular acidosis. Acetazolamide does this directly, but chemotherapy agents, aminoglycosides and others can cause proximal tubular damage that is leading to this effect.

Anyhow, whatever the cause, the treatment is Bicarbonate. Whereas in high anion gap met. acidosis HCO3 is generally contra-indicated, the opposite is true for normal anion gap acidosis. The patient is losing bicarb, so give him bicarb. He may need quite a bit. If the acidosis is severe, no less than 200-400 mmols of NaCO3 will be needed.

Naturally, it is imprtant to stop any medication that may be resonsible.

I would guess that the perforation was old, and was sealed with omentum, and that the chemotherapy was just enough to break the seal.